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[终末期及复苏后期脑亚细胞结构中的膜损伤]

[Membrane damage in brain subcellular structures in terminal states and in the postresuscitation period].

作者信息

Molchanova L V, Pylova S I, Zaks I O

出版信息

Biull Eksp Biol Med. 1983 May;95(5):17-9.

PMID:6850085
Abstract

Animal experiments were made to study and compare enzymatic activity of brain tissue mitochondria and microsomes treated and untreated with Tween-80 and Triton-X-100. In Mongolian gerbils, the 10-minute brain ischemia induced by bilateral carotid occlusion led to the labilization of the membranes of microsomal fractions, which did not return to normal an hour after resuscitation. The destructive effect of ischemia combined with clinical death from mechanical aspnyxia was similar to that of Triton-X-100. The ten-minute clinical death from ventricular fibrillation due to electroshock in dogs labilized lysosomal membranes. During the first hour after resuscitation and especially during the first 24 hours, the treatment of crude mitochondria with Tween-80 did not activate alkaline phosphatase and plasminogenic activator as compared with the control group.

摘要

进行动物实验以研究和比较用吐温 - 80和曲拉通 - X - 100处理和未处理的脑组织线粒体和微粒体的酶活性。在蒙古沙鼠中,双侧颈动脉闭塞诱导的10分钟脑缺血导致微粒体组分膜不稳定,复苏后1小时仍未恢复正常。缺血的破坏作用与机械性窒息导致的临床死亡相结合,其作用类似于曲拉通 - X - 100。狗因电击导致心室颤动的10分钟临床死亡使溶酶体膜不稳定。与对照组相比,复苏后第一小时尤其是最初24小时内,用吐温 - 80处理粗制线粒体并未激活碱性磷酸酶和纤溶酶原激活剂。

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